Cerebral hemorrhage in the elderly
Introduction
Introduction to cerebral bleeding in the elderly Cerebral hemorrhage (senilecerebralhaemorrhage) refers to cerebral arteries, veins or capillary rupture leading to bleeding in the brain parenchyma. According to the discipline and practicality, cerebral hemorrhage is divided into traumatic and non-traumatic. Traumatic cerebral hemorrhage is mainly discussed by neurosurgery. In non-traumatic cerebral hemorrhage, it is divided into secondary and primary cerebral hemorrhage. Secondary cerebral hemorrhage is caused by certain primary vascular disease, such as blood disease, connective tissue disease, brain tumor. , cerebral vascular malformations, cerebral vascular amyloidosis. Primary cerebral hemorrhage is based on arteriosclerosis. The rupture of the cerebral arteries leads to hemorrhage in the brain parenchyma. The cerebral hemorrhage caused by cerebral arteriosclerosis caused by hypertension is also called hypertension atherosclerotic cerebral hemorrhage or hypertensive Cerebral hemorrhage accounts for more than 80% of primary cerebral hemorrhage, which is more common in the elderly. basic knowledge The proportion of illness: 0.005% Susceptible people: the elderly Mode of infection: non-infectious Complications: pneumonia, acne, renal failure, stress ulcer, intracranial hypertension syndrome, hypertension, hypertensive crisis
Cause
Elder cerebral hemorrhage
High blood pressure (30%):
In cerebral hemorrhage patients, 90% of patients have high blood pressure. From cardiovascular research, it is found that 1/3 to 2/3 of hypertensive patients eventually have cerebral hemorrhage; hypertension does not undergo antihypertensive for a long time. Therapist, more than half of the cerebral hemorrhage occurs after 10 years, therefore, hypertension is the most important cause of primary cerebral hemorrhage. On the basis of hypertensive cerebral arteriosclerosis, when the mood is fluctuating or physical activity is excessive, the instantaneous blood pressure Increased, can cause cerebral vascular rupture leading to cerebral hemorrhage, and hypertension arteriosclerosis is a frequently-occurring disease in the elderly population, so cerebral hemorrhage is also one of the most common diseases in the elderly. This chapter only describes hypertensive arteriosclerotic cerebral hemorrhage. Hypertensive cerebral hemorrhage occurs in the arterial bean artery (also known as Charcot artery, hemorrhage artery) (Fig. 1), followed by the thalamic penetrating artery, the central branch of the basilar artery, etc. Hypertensive cerebral hemorrhage occurs in the basal ganglia Area, accounting for 70% of cerebral hemorrhage, brain stem is 10%, cerebellum is 10%, brain lobe is 10%, and in basal ganglia, shell nucleus bleeding accounts for 44%, thalamus is 13%, cerebral hemorrhage Symptoms are caused by hemorrhage, brain tissue compression, edema, displacement, softening and necrosis. Bleeding in the bottom section, often on the medial side, often invades the internal capsule and thalamus, and can also break into the lateral ventricle to fill the blood. Ventricular system and subarachnoid space (Fig. 2); on the lateral side, the hematoma directly breaks into the lateral fissure and the surface of the brain, causing subarachnoid hemorrhage, brainstem or cerebellar hemorrhage, can directly break into the subarachnoid space or In the fourth ventricle, the hematoma formed after cerebral hemorrhage causes the brain tissue to have an irregular cavity filled with purple-brown jelly-like fluid, and the surrounding area is a softening zone of necrotic edema; the surrounding tissue of the lesion is blocked by venous return and the softening zone occurs. Point hemorrhage, hematoma and edema cause the brain to change back The sulci is shallow; the ventricle is deformed by compression; in severe cases, the ipsilateral brain tissue is displaced to the opposite side or downward to form cerebral palsy. After that, the hematoma mass contracts and breaks, and the surrounding tissue edema gradually disappears; the hematoma fluid is absorbed. The cystic space is reduced, and the cystic cavity becomes a watery liquid containing yellowish hemosiderin. A layer of yellow-orange substance containing lutein is deposited on the wall of the cyst wall. The small amount of bleeding is filled by proliferating glial cells. . After the occurrence of cerebral hemorrhage, a series of pathological processes will occur, and the hematoma formed by cerebral hemorrhage depends on the condition of the hemorrhagic artery and surrounding brain tissue. Individuals may continue to bleed again in a short period of time, causing the hematoma to enlarge; most Because the ruptured arteries are quickly blocked and stop bleeding, a small amount of bleeding, blood permeates between the nerve fibers, does not destroy the brain tissue, can not produce any symptoms and signs, when the amount of bleeding often forms a large hematoma, can be within a few hours Lead to cerebral edema, plus a large hematoma, resulting in acute high intracranial pressure, so that the brain tissue is compressed, displaced or cerebral palsy, and due to local cerebral circulation disorders, causing hypoxia in the brain tissue, downward pressure on the thalamus, hypothalamus, Causes severe autonomic dysfunction, cerebral hemorrhage breaks into the ventricle or subarachnoid space, forming secondary ventricular hemorrhage or subarachnoid hemorrhage, cerebral hemorrhage breaks into the ventricles, especially when entering the fourth ventricle, resulting in an acute Obstructive hydrocephalus, intracranial pressure rises sharply, and cerebral palsy appears.
Brain-derived organ damage (15%):
Acute cerebral hemorrhage can indirectly or directly damage the hypothalamus, secondary neuroendocrine dysfunction, leading to functional damage of various organs; damage to the brain stem, causing vagus nerve dysfunction, directly leading to visceral dysfunction, therefore, cerebral hemorrhage in the acute phase Acute pulmonary edema, acute myocardial ischemia or infarction, acute pancreatic function damage caused by elevated blood glucose, renal dysfunction, gastric bleeding caused by gastric stress ulcer, etc., severe organ failure may occur due to acute encephalopathy The multiple organ failure caused by it is called brain-derived multiple organ failure. The death caused by this aspect accounts for 25% of cerebral hemorrhage. Active prevention and treatment of brain-derived multiple organ failure can effectively reduce the mortality of cerebral hemorrhage. .
Infection (15%):
As acute cerebral hemorrhage damages the neurological function of the cortex and hypothalamus, resulting in neuroimmune dysfunction, combined with severe paralysis, disturbance of consciousness and medullary paralysis, which together cause pulmonary-based infection.
Fever (10%):
Many patients develop fever and even high fever immediately after cerebral hemorrhage, which is caused by cerebral hemorrhage and the body temperature regulation center.
Prevention
Elderly cerebral hemorrhage prevention
Cerebral hemorrhage is one of the main causes of death and disability in the world. Strengthening research on prevention of cerebral hemorrhage has great significance for improving the health of the whole human being. Prevention is divided into primary prevention, secondary prevention, and tertiary prevention. prevention.
Primary prevention: It is a census and reasonable treatment of risk factors for curative cerebral hemorrhage in patients who have not had cerebral hemorrhage.
Secondary prevention: refers to the prevention of recurrent cerebral hemorrhage, can be treated with drugs, mainly to treat high blood pressure, lowering blood fat, regular health check, review blood lipids, hemodynamics, transcranial Doppler ultrasound, if necessary Head CT and cerebral angiography, early diagnosis, early treatment.
Tertiary prevention: mainly for the rehabilitation of complications and sequelae.
Risk factors and interventions for cerebral hemorrhage: Risk factors for cerebral hemorrhage are divided into several categories: Category 1 is a factor that cannot be changed, such as gender, age, etc.; Category 2 is an environmental factor, such as an infection or cold climate; The class is caused by an unhealthy lifestyle of the individual, including drug use, drinking, exercise, obesity, and unreasonable dietary structure; the fourth category is a disease that combines familial and environmental factors, such as hypertension, diabetes, except for the first Outside the category, the latter three categories can be changed through some intervention prevention measures.
Age is the most important risk factor for spontaneous cerebral hemorrhage, and its incidence increases significantly with age. Male cerebral hemorrhage is more common than females. Black Americans are more common than whites. This is due to the young and middle-aged American blacks. The incidence of bleeding is higher than that in Western countries. Hypertension is the most important risk factor for cerebral hemorrhage. In Japan, patients with hypertension were followed up for 14 years. It was found that the hypertension group had a 17-fold higher mortality than the normal blood pressure group. The vascular disease epidemiological survey showed that the risk of cerebral hemorrhage was significantly higher in patients with hypertension (OR, 13.62 for men and 11.36 for women); more incidence in winter than in other seasons; frequent tea and irritating food for the brain Hemorrhage has a protective effect, left ventricular hypertrophy can increase the risk of cerebral hemorrhage by 2 to 7 times. Intervention therapy has repeatedly shown that treatment of hypertension can significantly reduce the risk of cerebral hemorrhage; therefore, treatment of hypertension is recognized as the most effective for cerebral hemorrhage Interventions.
Other risk factors for cerebral hemorrhage that can be intervened include history of stroke, alcohol abuse, drug use, anticoagulant therapy, and thrombolytic therapy. One of the most important risk factors for cerebral hemorrhage in the elderly is vascular amyloidosis, but this can only be pathologically examined. Confirmed, MRI and genetic testing of Alzheimer's disease contribute to the diagnosis of cerebral hemorrhage caused by vascular amyloidosis. Other risk factors such as low serum cholesterol (<1.6g/L) and smoking require further study.
Complication
Elderly cerebral hemorrhage complications Complications pneumonia acne renal failure stress ulcer intracranial hypertension syndrome hypertension hypertensive crisis
Common complications include infections such as pneumonia, urinary tract infections, hemorrhoids, heart, kidney failure, and stress ulcers.
Symptom
Symptoms of cerebral hemorrhage in the elderly Common symptoms Intracranial high blood pressure brain stem bleeding Memory impairment Cerebellar hemorrhage Blood pressure drop Bridge cerebral hemorrhage Awareness disorder Ventricular hemorrhage Mental disorder Thalamic hemorrhage
The disease occurs mostly in middle-aged and elderly people, and can also occur in young people with high blood pressure. Most of them are active under the dynamic conditions such as agitation, fatigue, excessive exertion, etc.; a few people are sick under static or sleep, this situation is in the elderly Most of them have no premonition before cerebral hemorrhage, but very few patients have transient symptoms such as dizziness, headache, physical activity disorder or sensory disturbance several hours or days before bleeding.
After hypertensive intracerebral hemorrhage, the condition of most patients reaches a peak within a few minutes. The clinical manifestation depends on the amount and location of the bleeding. The typical manifestations of patients with moderate or higher bleeding are sudden dizziness, headache, and vomiting coffee. Substance, then there is a disturbance of consciousness or even a shallow coma, accompanied by flushing or pale, sweating, high blood pressure, slow pulse, incontinence, dilated pupils, slow photoreaction, straight brain, irregular breathing, etc. There may be unconscious and reactive movements of the limbs, while the affected limbs have no movement, a few patients have systemic convulsions, then enter a coma, with elevated body temperature, rapid and weak pulse, decreased blood pressure, dilated pupils, photoreaction disappears, limbs In a state of relaxation, etc., bilateral limb pain is irritating without reactive action, which may be life-threatening. A small amount of bleeding may manifest as a simple symptom or sign, or even asymptomatic and physical signs.
Basal ganglia hemorrhage
Blood pressure cerebral hemorrhage occurs well in the basal ganglia, and this area is the most common case of nucleus hemorrhage, which is caused by rupture of the bean vein artery. Because the nucleus hemorrhage often spreads to the internal capsule, it is often called clinically. For internal capsule bleeding, because the internal capsule is an important functional area, the damage of this part is mainly as follows:
(1) Hemiplegia of the contralateral limb: the muscle tension of the lateral limb is low, the tendon reflex declines or disappears, and even the pathological reflex is not induced. After several days or weeks, the paralyzed limb turns to an increased tension or spasm, the upper limb flexes and adducts, and the lower limb Straightening, sputum reflexes can lead to pathological reflexes.
(2) contralateral limb sensory disturbance: mainly pain loss.
(3) contralateral hemianopia: those who are conscious, can find contralateral blindness.
(4) gaze palsy: Most patients have persistent eyes to the bleeding side, but passively turn the head to the same side, the eyes can move to the opposite side, because the lateral center of the cerebral hemisphere is destroyed, making the eyes Can not move to the opposite side, this phenomenon disappears after 3 to 4 weeks of onset.
The above four kinds are the most common symptoms of cerebral hemorrhage, which can also be called four-biased symptoms. In addition, patients may also have aphasia, disuse, body image disorder, memory impairment, computational dysfunction, etc. The severity of symptoms depends on bleeding. The size of the amount, and whether it damages the hypothalamus and brainstem. When the amount of bleeding is large, it quickly enters a coma or even death. Without examination of limb paralysis and sensory disturbance, basal ganglia hemorrhage can be divided into medial and lateral hemorrhage, medial Type of bleeding is characterized by early and severe disturbance of consciousness. Patients often have disturbances of consciousness in the early stage of the disease, while hemiplegia is not heavy. When the lesion develops downward and affects the hypothalamus, the body temperature regulates the central disorder and appears hyperthermia; The blood sugar rises and urine sugar appears; the autonomous center suffers from stomach bleeding, arrhythmia, and sweating; the asymmetry of the eyeball occurs in the midbrain; the lateral hemorrhage is characterized by a lack of consciousness, and the "four biases" Symptoms are obvious, but if the amount of bleeding is large or bleeding continues, the condition may aggravate the performance of medial hemorrhage.
2. Thalamic hemorrhage
Mainly for the thalamic geniculate artery or thalamic penetrating artery rupture, the former is located in the lateral nucleus of the thalamus, the latter is located in the medial nucleus of the thalamus. The symptoms and severity of thalamic hemorrhage depend on the amount of bleeding, but the bleeding in this part has the following special which performed:
(1) Thalamic sensory dysfunction: hypothermia of the contralateral hemiplegia, hypersensitivity or spontaneous pain, Dejevine-Roussy syndrome.
(2) Thalamic aphasia: speech is slow and unclear, repeated speech, difficulty in pronunciation, poor retelling, but reading and reading normal, this aphasia is also a feature of cortical aphasia.
(3) Thalamic dementia: Chronic hemorrhage on one or both sides may cause memory loss, decreased computational power, affective disorder, personality disorder, and the like.
(4) Body image disorder: right thalamic hemorrhage may occur with hemiplegia and ignorance, partial agnosia and unilateral neglect.
(5) eye movement disorder: bleeding occurs in the medial part of the thalamus, posterior commissures and hypothalamus, there may be vertical eye movements, or gaze palsy.
If the amount of bleeding is large, in addition to the above symptoms, the surrounding brain tissue is compressed by the hematoma, and there is a clinical manifestation similar to the hemorrhage of the nucleus. If the amount of thalamic hemorrhage is small, there is no other manifestation other than sensory disturbance, and some symptoms and signs are also No, the amount of bleeding is medial cerebral hemorrhage, the condition is heavy, and the prognosis is poor.
3. Lobe bleeding
The rupture of the cerebral cortical artery can lead to cerebral lobe hemorrhage, or subcortical hemorrhage. Before the 1980s, cerebral hemorrhage was not serious due to illness, and there were few deaths, and the diagnosis was low. The statistical incidence was low. Since the 1990s, due to the extensive application of brain CT and MRI, the diagnosis of cerebral hemorrhage is more, so the incidence accounts for 15% to 20% of cerebral hemorrhage, and cerebral hemorrhage still accounts for hypertension. About 60%, other for cerebrovascular amyloidosis, cerebral vascular malformation, blood disease, anticoagulant therapy, skull base vascular network disease, etc., in addition to the usual common manifestations of cerebral hemorrhage, it is characterized by frequent bleeding More, the condition is not heavy, but the incidence of focal or systemic epilepsy is often, often manifested as a simple symptom or sign, the symptoms and signs of the brain lobe depends on the location of the bleeding, frontal hemorrhage may appear contralateral hemiplegia , motor aphasia and / or mental disorders, parietal hemorrhage is less hemiplegic, but partial sensation is significant, can be accompanied by contralateral lower quadrant blind, dominant hemisphere can appear sensory aphasia or mixed aphasia, temporal lobe Bleeding table Is on the side of the tongue and upper limb paralysis and contralateral based on quadrantanopia, there may be mixed dominant hemisphere aphasia, occipital lobe hemorrhage only showed contralateral hemianopia and macular evade phenomenon.
4. Brain stem bleeding
Primary brain stem hemorrhage accounts for about 10% of cerebral hemorrhage. In brain stem hemorrhage, the vast majority are cerebral hemorrhage, and a small part is midbrain hemorrhage. The medullary hemorrhage is extremely rare. The brain stem hemorrhage is mainly due to the paramedian artery. And the rupture of the short circumflex artery, its clinical manifestations and severity depends on the amount of bleeding.
(1) midbrain hemorrhage: sudden double vision, drooping eyelids, one or both pupils enlarged, different axes of the eye, horizontal or vertical nystagmus, ipsilateral limb ataxia, disturbance of consciousness, etc., also expressed as Weber or Benedikt syndrome, in severe cases, can go to a state of brain rigidity.
(2) Bridge cerebral hemorrhage: typical brain stem hemorrhage, its clinical manifestations are sudden headache, vomiting, dizziness, diplopia, nystagmus, different axes of the eye, cross-sensory disturbance, cross sputum, hemiplegia or quadriplegia; Then quickly enter the disturbance of consciousness, needle-like pupil, high fever, sweating, brain rigidity, difficulty breathing, etc.; may be accompanied by gastric bleeding, acute pulmonary edema, acute myocardial ischemia and even myocardial infarction, severe cases directly into the coma during the onset State, needle-like pupil, deafness, difficulty breathing, and associated with multiple organ damage, some of the cerebral hemorrhage can be expressed as some typical syndromes such as Foville, Millard-Gubler and atresia syndrome, before the 70s, It is believed that primary bridge cerebral hemorrhage is almost 100% dead, but due to the application of modern imaging, it is found that many of the cerebral hemorrhages are small. These patients sometimes present as single symptoms such as dizziness, diplopia, and a semi-integration. Symptoms, facial or limb numbness, unilateral or bilateral limb hemiparesis, etc., the prognosis is good, and some only leave lighter hemiplegia or ataxia, and some even return to normal.
(3) medullary hemorrhage: manifested as sudden stroke and coma, and soon died, some of the light may have double lower limb paralysis, hiccups, facial sensory disturbance or Wallenlberg syndrome.
5. Cerebellar bleeding
Accounted for 10% of cerebral hemorrhage, mainly due to rupture of the superior cerebellar artery, the inferior cerebellar artery or the posterior cerebellar arteries. As for which arterial hemorrhage occurs, there is no statistical analysis. The clinical manifestations of bleeding volume and location are different. Divided into the following three types:
(1) fulminant: about 20% of cerebellar hemorrhage, this type of patient is a large amount of hemorrhage in one side of the cerebellar hemisphere or ankle, the general amount of bleeding is above 15ml, the hematoma rapidly presses to the ventral side of the brainstem and causes high cranium Internal pressure, and finally lead to large occipital condyle, the patient showed sudden headache, vomiting, rapid coma, often died in the cerebral palsy within 1 to 2 days after the onset, due to the onset of illness quickly into coma, cerebellum and brain stem damage Symptoms and signs cannot be detected, so it is difficult to diagnose in an emergency.
(2) General type: about 70% of cerebellar hemorrhage, moderate cerebellar hemorrhage, 5 to 15 ml of bleeding, slow development of the disease, many patients can survive, cerebellum and brain stem damage can be detected, the patient suddenly Onset, manifested as headache, vomiting, dizziness, nystagmus, sputum eating and affected limb ataxia, consciousness is still clear, such as exacerbations, peripheral ipsilateral facial paralysis, nerve palsy, eyeball to the opposite side Oblique, corneal reflex disappeared, etc.; afterwards, some patients gradually developed disturbance of consciousness, pupil dilation and changes in vital signs.
(3) benign type: account for 10% of cerebellar hemorrhage, this type of patient is a small amount of cerebellar hemorrhage, the amount of bleeding is less than 5ml; or moderate amount of bleeding in the elderly, but because the brain of the elderly has different degrees of atrophy, therefore, hematoma occupying Sexual damage is not serious, symptoms are not obvious, prognosis is good, most patients show sudden vertigo, nausea and vomiting, with or without nystagmus, but generally without other signs, therefore, it is easy to be missed before brain CT examination Or misdiagnosis.
6. Ventricular hemorrhage (IVH)
The clinical manifestations are closely related to the location of ventricular hemorrhage, the amount of blood invading the ventricles and the extent of ventricular involvement. Secondary IVH also has clinical changes in primary lesions. Patients with mild IVH may be asymptomatic or have a little headache and vomiting. Severe IVH due to The blood enters the ventricle and causes cerebrospinal fluid circulation disorder. The abnormally increased intracranial hypertension often occurs, causing the brain stem to be compressed and distorted. The intraventricular hemorrhage secondary to thalamic hemorrhage often causes direct damage to the upper brain stem, so the performance is more dangerous. The mortality rate is high. The common clinical manifestations are: 1 severe headache, vomiting, rapid coma; 2 extremity convulsions or spasm, bilateral pathological reflexes, quadriplegia often flaccid, all tendon reflexes can not be induced, can also appear Paroxysmal tonic sputum, degenerative brain; 3 high fever, meningeal stimulation positive; 4 cerebrospinal fluid is bloody; 5CT examination of ventricular system and / or subarachnoid high-density changes, may have ventricular system expansion; 6 vital signs changes Obviously, if the breathing is deep, the rotation is slow and irregular, the pulse is slow, the force is fast, weak, irregular, and the blood pressure is unstable. In case of high fever, the condition is dangerous. According to the extent of bleeding, whether there is blood clot, clinical manifestations and prognosis are different. Pia study found that blood clots exist in the lateral ventricle or side ventricle and third ventricle. The coma and severe brainstem function are impaired, and the prognosis is poor. When the blood clot only affects one side of the ventricle or the ventricle is not a blood clot, the patient's consciousness disorder is mild and often survives.
Examine
Elderly cerebral hemorrhage examination
Blood test
In many patients with cerebral hemorrhage, especially in patients with severe cerebral hemorrhage, due to neurological or endocrine reasons, routine blood tests indicate increased white blood cells, elevated blood glucose, elevated blood urea nitrogen and non-protein nitrogen, elevated serum muscle enzymes, etc. It is the rise of blood leukocytes and blood sugar in more than half of patients, and more than 90% of patients with severe cerebral hemorrhage.
2. Urine examination
Urine tests for patients with partial cerebral hemorrhage found urine sugar and proteinuria.
3. Cerebral angiography
Before CT, it was an important diagnostic method for cerebral hemorrhage. In cerebral angiography, it mainly showed mass occupying position, such as basal cerebral hemorrhage. The anterior position of the anterior cerebral artery moved to the contralateral side, and the lateral fissure artery moved to the lateral side. The distance between the two increases, the lateral position is the downward displacement of the end of the internal jugular vein, the anterior cerebral artery is displaced upward, the lateral fissure artery is raised, the choroidal artery, the posterior communicating branch and the posterior cerebral artery are posterior. Shift down, etc.
4.CT scan
On CT, the development of cerebral hemorrhage depends on hemoglobin in the blood, and its X-ray absorption coefficient is significantly larger than that of brain tissue, so it has a high density shadow, and its density change evolves with time.
(1) In the hyperacute phase (onset to 24h), the fresh hemorrhage is whole blood, the hemoglobin is not high, and the brain tissue is mixed. The CT value is 50-60Hu, showing a higher density.
(2) In the acute phase (2-7 days), hemorrhage condenses into a blood clot, and hemoglobin increases significantly. The CT value is 80-90 Hu, showing a significant high-density shadow.
(3) Hemoglobin and fibrin decompose in the subacute phase (8 to 30 days), and the high-density hematoma gradually shrinks toward the center of the heart, and the periphery shows a high density shadow.
(4) During the recovery period (5-8 weeks), the hemorrhage block was completely dissolved and absorbed. The hemorrhagic lesion was yellow liquid and softened. The CT showed low density and the boundary was not clear.
(5) The cystic period (more than 2 months) is liquid, similar to cerebrospinal fluid, CT value 010Hu, low-density shadow, clear boundary, early hematoma of cerebral hemorrhage, varying degrees of brain edema around, occupying place Sexual, adjacent ventricle, cerebral cistern and sulcal pressure are narrowed or displaced. Later, hematoma and cerebral edema are gradually absorbed, and the place is reduced. The ventricles and cerebral cisterns are destroyed and return to normal position. When the hematoma and cerebral edema are completely dissipated. Secondary gliosis, brain softening and brain atrophy, local cerebral ventricle, cerebral cistern and sulcal local compensation to expand, and shift to the lesion, close to the cerebral cerebral hemorrhage, can break into the ventricle, CT can often show Broken into the site, intraventricular hematoma distribution and content, a small amount of intraventricular hemorrhage, accumulation in the lateral chamber triangle and occipital region, and cerebrospinal fluid can be a contour plane, a large number, intraventricular lumps hematoma or full brain outdoor system It is a high-density cast of the brain, and the ventricles can be enlarged.
For cerebral hemorrhage with unknown cause, it is feasible to enhance CT scan identification, cerebral hemorrhage for more than 1 week, granulation tissue formation at the edge of hematoma, showing ring enhancement, shape and size consistent with hemorrhage hematoma, sustainable for 4 to 6 weeks, in enhanced CT On the electric scan, it showed edema around the circumference, ring enhancement, liquefied hematoma and central clot, etc., which is the CT manifestation of the typical hematoma absorption period.
5.MRI scan
The main factors of MRI imaging of cerebral hemorrhage are not only related to hemoglobin content, but more importantly, the traits of iron contained, iron is a paramagnetic substance, so the evolution of hematoma is mainly the evolution process of various hemoglobin hemosiderin. Determine the MRI signal performance. On MRI, cerebral hemorrhage can be divided into 4 layers: the central core layer, the most hypoxic; the outer nuclear outer layer, the hypoxia is lighter; the outer edge layer, the phagocytic cells Hemosiderin; the most external reaction zone, cerebral glial hyperplasia and varying degrees of cerebral edema, due to the destruction of the blood-brain barrier, it is angiogenic finger cerebral edema.
(1) Hyperacute period (onset to 24h) Hematoma is similar to whole blood, mainly oxyhemoglobin, non-paramagnetic, proton-free and T2 relaxation enhancement effect. On MRI, T1 is equal or slightly higher signal, T2 is slightly higher Or mixed signals, no long T1 around the hematoma, long T2 edema.
(2) In the acute phase (2-7 days), clot formation, mainly deoxyhemoglobin, paramagnetic, M1 on T1 is equal or slightly lower signal, T2 is low signal, and the periphery of the hematoma is long T1 and T2 edema.
(3) In the subacute phase (8 to 30 days), the hematoma is mainly methemoglobin, paramagnetic, and has proton relaxation enhancement effect, so T1 and T2 are shortened, and hematoma serotonin is increased on the edge of hematoma. On MRI, The stratification of typical hematoma, in the weighted T1, T2 and proton density, is characterized by a central low and high peripheral signal.
(4) In the recovery period (5-8 weeks), the hematoma is basically absorbed, mainly methemoglobin, free state, M1, T1, T2 and proton density are all high signals, surrounded by hemosiderin deposition signal black ring.
(5) The cystic period (more than 2 months) hematoma dissolution and absorption, mainly free methemoglobin, surrounded by a large amount of hemosiderosis, MRI, the lesion area is T1, T2 high signal, surrounded by low signal ring, Cerebral edema disappeared. If it contains a cerebrospinal fluid cyst, it is low in T1 and high in T2.
MRI is superior to CT in that it is easy to display small and more concealed hemorrhage, for example, brain stem hemorrhage and cerebellar hemorrhage, in addition to common cerebral arteriosclerosis and hypertensive cerebral hemorrhage, cerebral hemorrhage caused by cerebral vascular malformation It can also show the airflow effect of deformed blood vessels, making the cause diagnosis more accurate and reliable.
6. Waist wear check
If there is no condition or can not carry out brain CT scan, lumbar puncture should be performed to help diagnose cerebral hemorrhage, but the positive rate is about 60%, and there is a certain false positive rate. When cerebral hemorrhage breaks into the ventricle or subarachnoid space, waist Wearing blood cerebrospinal fluid examination, at the same time, can also detect intracranial pressure, which is helpful for guiding dehydration treatment. However, if there is a large amount of bleeding or cerebral palsy, be careful to do a lumbar puncture to avoid cerebral palsy.
7. EEG
It can be suggested that there is a slow wave in the cerebral hemorrhage, but it is not specific
8. Electrocardiogram
About half of the patients with cerebral hemorrhage have different degrees of arrhythmia or myocardial ischemia, and even myocardial infarction. Electrocardiogram can be used to understand the heart condition, early detection and timely treatment.
Diagnosis
Diagnosis and diagnosis of cerebral hemorrhage
diagnosis
The clinical diagnosis of cerebral hemorrhage in the elderly is the most premature aging, with a history of previous hypertension, often in the onset of mental or physical labor, rapid progression of the disease, increased cerebrospinal fluid pressure, more bloody, CT, MRI can confirm the diagnosis .
Differential diagnosis
1. Identification of cerebral hemorrhage and subarachnoid hemorrhage
Subarachnoid hemorrhage is often accompanied by severe headache, vomiting and obvious meningeal irritation, no or lighter disturbance of consciousness, few signs of localized nervous system, cerebrospinal fluid is bloody, plus CT, MRI, generally not Difficult to identify.
2. Cerebral hemorrhage and aneurysm, differential diagnosis of arteriovenous malformation
Aneurysms and arteriovenous malformations generally have a young age of onset, and hemorrhage directly enters the subarachnoid space. Therefore, meningeal irritation signs appear first, followed by hemiplegia and other manifestations. CT, MRI and cerebral angiography can be identified.
3. The identification of cerebral hemorrhage and brain death
Because cerebral hemorrhage and cerebral infarction are different in treatment, the identification is very important. Patients with cerebral infarction often have a state of rest and rest. There are many transient ischemic attacks before the onset, and the disturbance of consciousness is mild or not after the onset. Focal signs are heavier, cerebrospinal fluid pressure is not high and colorless and transparent, clinical application of CT, MRI, identification has been very easy.
